| ObjectiveTo observe the effect of recombinant human erythropoietin(rHuEPO) on the number of apoptosis and neurons, and the expression ofheat shock protein (HSP) 72 in the retina of Sprague-Dawley rats withretinal ischemia-reperfusion (RIR) injury.MethodsFirstly, totally 18 SD rats were divided randomly into normalcontrol group (n=6), RIR group(n=6), sham operation group (n=6), themodel of RIR injury was induced by increasing intraocular pressure viaan intracameral catheter, the pressure was 110 mmHg, maintaining 1hour. Animals were sacrificed at 24 hours after reperfusion. The resultswere evaluated by histopathological examination and TdT-mediatedbiotin-dUTP nick end labeling (TUNEL) staining. In addition, apoptosiscells were counted and analysed statistically.Secondly, totally 78 Sprague-Dawley rats were divided randomlyinto normal control group (n=6), RIR injury group(n=24), EPOtreated group (n=24, rats in this group were injected with rHuEPO intoabdominal cavity ) and quercetin group(n=24), and the right eye waschosen as experimental eye. Immunohistochemists technique and TUNELstaining technique was used to examine the expression of HSP72 and the apoptosis of retinal cells and the architecture of the retina were measuredby HE staining method before and 12, 24, 48, 72hours after reperfusion,respectively.Results(1) The number of apoptotic cells were different. In normal controlgroup and sham operation group,there were 0.83±0.753/HP and1.00±0.632/HP respevtively. But in RIR injury group, there were30.334±2.160/HP(p＜0.01).(2) The expression of HSP72 in the retina of normal control groupwas weak, after RIR injury the HSP72 expression began to increase at12h of reperfusion and peaked at 24h, then gradually decreased. Theexpression of HSP72 of EPO group was higher than RIR injury group,Quercetin group at 12h, 24, 48h after reperfusion(p＜0.05).(3) Very few apoptosis cells were seen in the rat retina of normalcontrol group. In every experimental group, the apoptosis cell began toincrease at 12h after reperfusion and peaked at 24h, then graduallydecreased after 48h. The apoptosis cells were more than normal controlgroup at each time of reperfusion, and the apoptosis cell of EPO treatedgroup is less than RIR injury group, quercetin group at each time ofreperfusion(p＜0.05).(4) After reperfusion, the internal retina became edema in RIRinjury group, quercetin group, and gradually the structure of retina was destroyed, the retina of EPO treated group is relatively complete.Conclusions(1) Established RIR injury model successfully by increasingintraocular pressure via an intracameral catheter.(2) The phenomenon of apoptosis is obvious in the retina afterischemia-reperfusion injury.(3) The expression of HSP 72 in the retina of normal control grouprats is very weak. Ischemia -reperfusion injury can induce HSP 72expression. Intraperitoneal injection EPO to the rat can obviously inducethe expression of HSP 72 in the retina of rat.(4) EPO can obviously deduce the apoptosis cell which was inducedby the injury of RIR, and sustain the retinal morphous.(5) EPO can protect the retinal neuron after RIR injury by icreasingthe expression of HSP72.
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